Illustration of a healthy neuron (left) showing a microtubule and tau proteins (green). The neuronal degeneration with the build-up of hyperphosphorylated tau proteins (yellow) is shown on the right. / picture alliance
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Uppsala – A single sleepless night in young adults in blood plasma causes an increase in tau protein, the deposition of which in the brain is a key hallmark of Alzheimer’s disease and other neurodegenerative diseases. The clinical importance of in Neurology (2019; DOI: 10.1212 / WNL.0000000000008866) published results is unclear.
Tau proteins are a normal part of neurons. When the nerve cell decays, they form aggregates called tau fibrils. Some tau proteins are drained into the cerebrospinal fluid via the glyphatic system, the brain’s lymphatic system, which was discovered only a few years ago. With modern detection methods, tau proteins can also be detected in plasma. The same applies to the components of beta amyloid and other brain molecules.
Previous studies have shown that sleep deprivation in the elderly leads to an increase in cerebrospinal fluid tau proteins. This is interesting because many Alzheimer’s patients suffer from sleep disorders. It is unclear whether the sleep disorders are the cause or the consequence of the dew deposits.
A team led by Jonathan Cedernaes from the University of Uppsala can now show that even in younger people there is an increase in tau proteins in the blood after a sleepless night. 15 healthy men aged 22 years and older participated in the study.
The subjects spent 2 days and 2 nights in a sleep laboratory in 2 study phases. In the first phase of the study, they received their usual sleep both nights. In the second phase of the study, they were asked not to sleep on the second night.
Deprivation of sleep led to a 17.2% increase in tau proteins in the subjects the next morning. After the nights of normal sleep, the plasma value only increased by 1.8%. The researchers also determined the concentration of beta-amyloids Abeta40 and Abeta42 as well as the neurofilament light chain (NfL) and the acidic glia fiber protein (GFAP). There was no increase in these brain molecules after the woke-up night.
According to Cedernaes, the results do not necessarily mean that sleepless nights are a risk factor for dementia in young adulthood. It is quite possible that the increase in tau proteins can only be attributed to increased neuronal activity during the nocturnal waking phase. The next step could be to investigate how long the rise in tau proteins continues after a night of sleep and how longer disturbances in the day-night rhythm have an effect. Long-term epidemiological studies would have to investigate whether sleep disorders in the younger age increase the risk of dementia in the long term. © warmth / aerzteblatt.de
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